作者：Albert; FERROmobilizationprogenitorepcsstreptozotocincirculatingcytometryrestorationunderlyingsuppressed
摘要：<正>Objective The aim of the present study was to explore potential mechanism underlying reduced basal circulating endothelial progenitor cells (EPCs) in diabetes, and to determine how diabetes impairs ischemia-induced mobilization of bone marrow-derived EPCs. Methods Circulating c-Kit+/Sca-1+/flk-1+ EPCs and CD31bright/Annexin V+ endothelial microparticles (EMPs) were analyzed by flow cytometry in control and streptozotocin-induced diabetic C57BL/6 mice. Results Compared with nondiabetic controls, diabetic mice had lower level of circulating EPCs, higher level of plasma EMPs, and increased ratio of EMPs to EPCs. Circulating EMPs count and EPCs level were negatively associated with each other. In a hindlimb ischemia model, diabetes suppressed bone marrow-derived EPCs mobilization, accompanied by insufficient upregulaiton of vascular endothelial growth factor (VEGF) and over-activation of matrix metalloproteinases (MMPs) system. As a consequence, diabetic mice showed deficient increase of capillary density and hampered restoration of transcutaneous oxygen pressure (tcpO2) in the ischemic tissue.Concluslon These results suggest that lower circulating EPCs level detected in diabetes may be partly attributed to consumptive loss of EPCs due to increased endothelial damage. Impairment in ischemia-induced EPCs mobilization presents a novel mechanism for defective post-ischemia neovascularization in diabetes.
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